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由细菌细胞壁中的关节病肽聚糖 - 多糖聚合物诱导产生的免疫抑制性巨噬细胞。

Immunosuppressive macrophages induced by arthropathic peptidoglycan-polysaccharide polymers from bacterial cell walls.

作者信息

Regan D R, Cohen P L, Cromartie W J, Schwab J H

机构信息

Department of Microbiology, School of Medicine University of North Carolina Chapel Hill 27514.

出版信息

Clin Exp Immunol. 1988 Dec;74(3):365-70.

Abstract

Rats injected with peptidoglycan-polysaccharide polymers derived from group A streptococcal cell walls (PG-APS) develop a chronic, remittant, erosive synovitis. Spleen cells from injected rats failed to proliferate when stimulated in vitro by Con A or PHA, unless nylon wool adherent cells were first removed. The suppression could also be reversed by removing phagocytic cells which had ingested carbonyl iron. Cells from control rats were suppressed in vitro by co-culture with unfractionated or nylon wool-adherent cells from PG-APS injected rats, and the suppressor activity was still expressed after exposure of the suppressor cells to 3,000 rad of irradiation. Addition of catalase and indomethacin to cultures only partially reversed the suppression. T lymphocytes from rats given a single arthropathic dose of PG-APS remained suppressed for at least 86 days after injection. Cells from rats given a low, non-arthropathic dose of PG-APS did not become suppressed. Cells from the Buffalo rat, which is resistant to development of PG-APS-induced chronic arthritis, showed less suppression than cells from the susceptible Lewis and Sprague-Dawley rat strains.

摘要

注射了源自A组链球菌细胞壁的肽聚糖 - 多糖聚合物(PG - APS)的大鼠会发展出一种慢性、缓解性、侵蚀性滑膜炎。除非首先去除尼龙毛黏附细胞,否则注射大鼠的脾细胞在体外受到刀豆蛋白A(Con A)或植物血凝素(PHA)刺激时不会增殖。通过去除摄取了羰基铁的吞噬细胞也可以逆转这种抑制作用。对照大鼠的细胞在体外与来自注射PG - APS大鼠的未分级或尼龙毛黏附细胞共培养时会受到抑制,并且在将抑制细胞暴露于3000拉德辐射后,抑制活性仍然存在。向培养物中添加过氧化氢酶和吲哚美辛只能部分逆转这种抑制作用。给予单次致关节炎剂量PG - APS的大鼠的T淋巴细胞在注射后至少86天仍受到抑制。给予低剂量、非致关节炎剂量PG - APS的大鼠的细胞没有受到抑制。对PG - APS诱导的慢性关节炎发展具有抗性的布法罗大鼠的细胞,其抑制作用比易感的刘易斯和斯普拉格 - 道利大鼠品系的细胞要小。

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